In a normal human heart, the sinus node, generally located near the junction of the superior vena cava and the right atrium, constitutes the primary natural pacemaker initiating rhythmic electrical excitation of the heart chambers. The cardiac impulse arising from the sinus node is transmitted to the two atrial chambers, causing a depolarization known as a P-wave and the resulting atrial chamber contractions. The excitation pulse is further transmitted to and through the ventricles via the atrioventricular (A-V) node and a ventricular conduction system causing a depolarization known as an R-wave and the resulting ventricular chamber contractions.
The intrinsic heart rate is primarily controlled by the sympathetic and parasympathetic components of the autonomic nervous system. Both components have nerve fibers terminating on the sinus node. Increased sympathetic activation (increased sympathetic tone) increases the heart rate as well as the conduction velocity of action potentials through the heart. Increased parasympathetic tone, also referred to as “vagal tone” since the parasympathetic nerves enter the heart via the vagus nerve, decreases the heart rate and decreases conduction velocity through the heart. Other factors such as circulating hormones and heart wall stretch will also influence heart rate and conduction. Though not fully understood, cardiovascular diseases and other physiological states may alter sympathetic tone, parasympathetic tone, and circulating hormonal levels and thus alter the heart tissue conduction velocity.
Disruption of the natural pacemaking and conduction system as a result of aging or disease can be successfully treated by artificial cardiac pacing. Implantable cardiac stimulation devices, including pacemakers and implantable defibrillators, deliver rhythmic electrical pulses or other anti-arrhythmia therapies to the heart at a desired energy and rate via electrodes implanted in contact with the heart tissue. One or more heart chambers may be electrically stimulated depending on the location and severity of the conduction disorder.
Cardiac stimulation devices have a great number of adjustable parameters that must be tailored to a particular patient's therapeutic needs. The process of selecting the optimal parameter settings can be lengthy and complicated. Recent clinical evidence supports the use of multichamber stimulation devices for improving hemodynamic efficiency in patients with congestive heart failure. With an increasing number of indications for cardiac pacing, the number of programmable parameters required for tailoring individual patient therapies further complicates the programming process.
Without feedback on the effect of programmed parameters, the physician faces a challenge in selecting the most effective pacing regimen. It would be advantageous, therefore, to provide the physician with physiological data that reflects the effect of an applied therapy, whether the therapy is an implanted stimulation device or a drug therapy.
Observation of changes related to sympathetic and vagal tone, which are known to occur with certain disease processes, may be one way to monitor the response to a therapy. For example, high, relatively constant sympathetic tone and low vagal tone are known chronic conditions in patients with heart failure. Unusual circadian changes in myocardial conduction velocity may be observed in patients with heart failure. Long-term monitoring of myocardial conduction velocity, therefore, would allow conduction changes to be detected that might be indicative of a change in heart condition. This monitoring would allow tracking of disease progression or the response to drug therapy or programmed pacing parameters.
A method for adjusting pacemaker parameters based on a measured myocardial conduction time has been proposed; however, the adjustments are made based on relatively short-term changes in conduction time, for example a change measured over three cardiac cycles. Since the physiological response to a change in drug therapy or programmed pacing parameters may not be instantaneous but may occur over an extended period of time, long-term monitoring of a physiological parameter reflective of the heart condition is desirable.
A device and method for long-term monitoring of myocardial conduction velocity, therefore, would improve the physician's ability to monitor a patient's disease state or therapy response. Such a method would preferably allow myocardial conduction data to be collected in an ongoing, day-to-day basis during a patient's normal activities. A physician may then examine the collected data for any shifts in long-term average myocardial conduction velocity and use this information in diagnosing the patient's heart condition and selecting treatments.